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Obesity childhood is related to vitamin D deficiency, but the mechanisms for this association still remain questionable. We hypothesized that behavioral factors would be decisive in reducing the body content of vitamin D in patients with obesity. A cross-sectional clinical and analytical study (calcium, phosphorus, calcidiol, and parathyroid hormone) was carried out in a group of 377 patients with obesity (BMI-DS >2.0), 348 patients with severe obesity (BMI-DS >3.0), and 411 healthy children. The place of residence was categorized as urban or rural. Vitamin D status was defined according to the US Endocrine Society criteria. The prevalence of vitamin D deficiency was significantly higher (p < 0.001) in severe obesity (48.6%) and obesity groups (36.1%) than in the control group (12.5%). Vitamin D deficiency was more frequent in severe obesity and obesity groups living in urban areas than in those living in rural areas (not in the control group). The patients with obesity living in urban residence did not present significant seasonal variations in vitamin D deficiency throughout the year in contrast to those patients with obesity living in rural residence. These findings suggest that the most probable mechanism for vitamin D deficiency in children and adolescents with obesity, rather than altered metabolic, is the behavioral factors (sedentary lifestyle and lack of adequate sunlight exposure).
Department of Pediatrics, School of Medicine, University of Navarra, Spain
Department of Pediatrics, Navarra University Hospital, Spain
Navarrabiomed (Biomedical Research Center), Spain
Fidel Gallinas-Victoriano
Department of Pediatrics, Navarra University Hospital, Spain
Navarrabiomed (Biomedical Research Center), Spain
*Address all correspondence to: tdura@unav.es
1. Introduction
Vitamin D is currently assigned a pleiotropic profile [1, 2, 3]. In point of fact, basically every human tissue and cell contains vitamin D receptors, and its biological effects are categorized as skeletal (bone metabolism and calcium homeostasis) and extra-skeletal (hypovitaminosis D appears to be involved in autoimmune diseases, infections, neuropsychiatric disorders, cardiovascular risk, prostate and breast cancer, etc.), a circumstance that justifies the interest in monitoring its body content.
Furthermore, the prevalence of childhood obesity has gradually increased in the course of the last decades, establishing as the most relevant nutritional disorder in our environment [4, 5, 6]. Even though obesity is considered as a multifactorial disorder, the celerity of its increase in prevalence is related essentially to behavioral factors: scarce healthy nutrition habits as well as a sedentary lifestyle conditioned, in large part, by new technologies (screen time, including television viewing, use of computers and video games) [7, 8].
Several studies have demonstrated that obesity childhood is related to vitamin D deficiency [9, 10, 11, 12]. The main source of vitamin D is the exposure to natural sunlight (cutaneous synthesis through ultraviolet B radiation) and, therefore, the higher prevalence of vitamin D deficiency in children and adolescents with obesity could be secondary to a more sedentary lifestyle (less mobility and participation in outdoor activities) and, consequently, a lack of adequate sun exposure. However, many explanations have been proposed for this association, but, interestingly, they hardly introduce theoretical mechanisms that imply limited sun exposure: storage or sequestration in adipose tissue, volumetric dilution, impaired hepatic 25-hydroxylation, etc. [3, 13, 14, 15, 16].
The main causes of vitamin D deficiency are generally ascribed either to some physical agent that obstructs solar radiation (clothing, sunscreen, etc.) or to geographical characteristics, such as latitude and season of the year, cloudy weather, altitude, etc. [2, 17]. In fact, recent studies using an objective and accurate method for ultraviolet radiation monitoring in children and adolescents have revealed that rural residents receive higher levels of ultraviolet radiation exposure than urban residents do [18, 19].
This study aims to compare vitamin D status between children and adolescents with obesity living in an urban area and in a rural area in Navarra, Spain (latitude between 43°16″42 and 41°55″22 North). We hypothesized that behavioral factors (outdoor activities and sun exposure) would be decisive in reducing the body content of vitamin D in patients with obesity.
We conducted a cross-sectional study in a group of 377 patients, aged 6.50–15.7 years, previously diagnosed with obesity (obesity group, BMI-DS >2.0, 97th percentile) and 348 patients, aged 7.4–15.3 years, diagnosed with severe obesity (severe obesity group, BMI-DS >3.0, 99th percentile). The participants were assessed in a clinical evaluation in the Pediatric Endocrinology Unit in this hospital in January 2014–December 2021. Clinical features (sex, age, season of study visit, place of residence, and BMI) and blood testing data (calcium, phosphorus, calcidiol, and PTH) were collected. Tanner’s classification was used for the assessment of pubertal staging, and the individuals were subsequently classified in school subgroup (Tanner stage I) and adolescent subgroup (Tanner stages II–V). Additional classification based on the place of residence (population or the city, higher or less than 10,000 inhabitants, respectively) was made, establishing urban or rural subgroups.
These features and measurements (clinical examination and blood testing) were estimated in a control group made up of 411 healthy children, aged 7.1–14.9 years, with BMI-DS in a range of −1.0 (15th percentile) to +1.0 (85th percentile).
Every participant in the study was Caucasian and lived in Navarra, Spain. Clinical records were surveyed in order to exclude any condition that could affect bone health, or any chronic pathology that could affect growth, body composition, food ingestion, or physical activity, or the previous intake of any medication (antiepileptic drugs or glucocorticoids), vitamin D, or calcium supplements.
2.2 Clinical examination
A previously published standardized protocol was applied for the anthropometric measurements [20]: participants were placed in underwear and barefoot, and we used an Año-Sayol scale (reading interval 0–120 kg and a precision of 100 g) for weight measures, and a Holtain wall stadiometer (reading interval 60–210 cm, precision 0.1 cm) for height measures.
The program Aplicación Nutricional, from the Spanish Society of pediatric gastroenterology, hepatology, and nutrition (Sociedad Española de Gastroenterología, Hepatología y Nutrición Pediátrica, available at http://www.gastroinf.es/nutritional/) was used to calculate the standard deviation (DS) values for the BMI. The graphic charts from the study of Ferrández et al. (Centro Andrea Prader, Zaragoza 2002) were used as the reference pattern [21].
2.3 Blood testing
The blood sample for biochemical determinations (calcium, phosphorus, 25(0H)D, and PTH) was obtained in basal fasting conditions (between 8:00 h and 9:00 h after an overnight fast).
The medical device used for the determination of calcium and phosphorous plasma levels was a COBAS 8000 analyzer (Roche Diagnostic, Mannheim, Germany). The determination of calcidiol levels was made with a high-specific chemiluminiscence-immunassay (LIAISON Assay, Diasorin, Dietzenbach, Germany), and the determination of PTH levels using a highly specific solid-phase, two-site chemiluminescent enzyme-labeled immunometric assay in an Immulite analyzer (DPC Biermann, Bad Nauheim, Germany).
The criteria of the United States Endocrine Society [22, 23] were applied to distribute individuals according to vitamin D plasma levels. In this way, a determination of calcidiol plasma level below 20 ng/ml (<50 nmol/L) was considered vitamin D deficiency, calcidiol plasma levels between 20 and 29 ng/ml (50–75 nmol/L), vitamin D insufficiency, and concentrations equal to or higher than 30 ng/ml (> 75 nmol/L) vitamin D sufficiency.
2.4 Statistical analysis
Tables show the results as percentages (%) and means (M) with corresponding standard deviations (SD). The program Statistical Packages for the Social Sciences version 20.0 (Chicago, IL, USA) was used to perform the statistical analysis (descriptive statistics, Student’s t-test, analysis of variance, χ2 test, and Pearson’s correlation). Statistical significance was assumed when P value was <0.05.
Parents and/or legal guardians were informed and provided consent for the participation in this study in all cases. This study was approved by the Ethics Committee for Human Investigation at our institution (in accordance with the ethical standards laid down in the 1964 Declaration of Hensinki and later amendments).
Table 1 shows and compares the distribution of demographic features in the severe obesity, obesity, and control groups. No significant differences were found in the distribution in relation to sex, age group, season of blood sample collection, and place of residence.
Distribution of geographic/demographic features in severe obesity, obesity, and control groups.
Chi2.
The mean values for age in the severe obesity, obesity, and control groups were 11.4 ± 2.9, 11.3 ± 2.7, and 11.1 ± 2.5 years, respectively, and there were no significant differences (p = 0.650) in age between the different groups. Obviously, the mean values for BMI-SD were significantly higher (p < 0.001) in the severe obesity (4.27 ± 1.28) and obesity groups (2.48 ± 0.28) with respect to control group (0.24 ± 0.23).
Figure 1 depicts and compares the prevalence of vitamin D status in the control, obesity, and severe obesity groups. The prevalence of vitamin D deficiency was significantly higher (Chi2: 159.8, p < 0.001) in severe obesity (48.6%) and obesity groups (36.1%%) than in the control group (12.5%). That is, only 12.2% and 16.2% of patients of the severe obesity and obesity groups showed levels of 25 (OH)D higher than 30 ng/mL, respectively, in contrast to 42.6% of the participants in the control group (p < 0.01).
Figure 1.
Prevalence of vitamin D status in control, obesity, and severe obesity groups.
Table 2 shows and compares the mean values for biochemical determinations in both groups in accordance to vitamin D status. There were not any significant differences in calcium and phosphorus levels between the different groups of vitamin D status, and obviously 25(OH)D levels were significantly lower (p < 0.001) in vitamin D insufficiency and deficiency individuals than in vitamin D sufficiency individuals in each group. PTH levels were significantly higher (p < 0.001) in the group with vitamin D insufficiency and deficiency than in vitamin D sufficiency within each group. In addition, there were not any significant differences in calcium, phosphorus, and 25(OH)D levels in each vitamin D status group between the different groups. However, PTH levels were significantly higher (p < 0.001) for each vitamin D status in the severe obesity and obesity groups with respect to the control group.
Biochemical determinations according to vitamin D status in severe obesity, obesity, and control groups (M ± SD).
ANOVA.
ANOVA between groups (p < 0.001).
Figure 2 presents and compares the prevalence of vitamin D deficiency according to the seasons of the year between control, obesity, and severe obesity groups. In each group, the highest prevalence of vitamin D deficiency (Chi2: 65.01, p < 0.001) corresponded to winter (severe obesity group: 65.1%, obesity group: 40.4%, and control group: 19.5%), and they reached a minimum in the summer (severe obesity group: 26.7%, obesity group: 26.1%, and control group: 3.8%). The prevalence of vitamin D deficiency in the different seasons of the year was significantly higher (p < 0.001) in the severe obesity and obesity groups with respect to the control group.
Figure 2.
Prevalence of vitamin D deficiency according to the seasons of the year in control, obesity, and severe obesity groups.
Figure 3 exposes and compares the prevalence of vitamin D deficiency in relation to the place of residence between control, obesity, and severe obesity groups. In the control group, there were no significant differences (p = 0.466) in vitamin D deficiency between urban (14.7%) and rural (10.5%) subgroups. As for the obesity group, vitamin D deficiency was significantly more frequent (p < 0.01) in the urban (48.6%) than in the rural subgroup (24.1%); additionally, in the severe obesity group, also vitamin D deficiency was significantly more frequent (p < 0.01) in the urban (61.3%) than in the rural subgroup (36.9%).
Figure 3.
Prevalence of vitamin D deficiency in relation to the place of residence in control, obesity, and severe obesity groups.
Figure 4 displays and compares the prevalence of vitamin D deficiency according to the seasons of the year between the individuals in the control, obesity, and severe obesity groups that lived in urban residence. In the control group, there were significant seasonal variations (Chi2: 38.1, p < 0.01) in vitamin D deficiency, which showed the lowest prevalence of vitamin D deficiency during the summer (7.1%) and the highest during the winter (25%). In contrast, there were no significant seasonal variations in the prevalence of vitamin D deficiency throughout the year in both the severe obesity and obesity groups. In fact, in severe obesity group, the prevalence of vitamin D deficiency during the summer was 51.6% and during the winter 67.6% (Chi2: 9.1, p = 0.170), and within the obesity group, vitamin D deficiency was 47% in the summer and 49.6% in the winter (Chi2: 9.2, p = 0.161).
Figure 4.
Prevalence of vitamin D deficiency according to the seasons of the year in individuals in the control, obesity, and severe obesity groups that lived in urban residence.
Figure 5 shows and compares the prevalence of vitamin D deficiency according to the seasons of the year between the participants in the control, obesity, and severe obesity groups that lived in rural residence. All groups presented significant seasonal variations in vitamin D deficiency throughout the year. In each group, the lowest prevalence of vitamin D deficiency corresponded to summer, and they reached a maximum in the winter. In severe obesity group, the prevalence of vitamin D deficiency during the summer was 9.1% and during the winter 57.1% (Chi2: 50,1, p < 0.01). In obesity group, vitamin D deficiency was 7.7% in the summer and 33.3% in the winter (Chi2: 21,9, p < 0.01). And, finally, in the control group, vitamin D deficiency was 0.0% during the summer and 10.4% during the winter (Chi2: 27,9, p < 0.01).
Figure 5.
Prevalence of vitamin D deficiency according to the seasons of the year in participants in control, obesity, and severe obesity groups that lived in rural residence.
A negative correlation (p < 0.01) between calcidiol and PTH levels (r = −0.375) was detected. In addition, a positive correlation (p < 0.01) between PTH and BMI-SD (r = 0.345) and a negative correlation (p < 0.01) between calcidiol and BMI-SD (r = −0.363) were observed.
This study verifies that vitamin D deficiency is a common condition in children and adolescents with obesity. Furthermore, our data suggest that this higher prevalence of vitamin D deficiency in these patients could be ascribed to inadequate sunlight exposure, since there was a weaker trend to vitamin D deficiency in those patients living in rural areas than in those living in urban areas.
Different geographic/demographic specificities, such as gender, age, season, or place of residence, have been described as factors associated with vitamin D deficiency [9, 10, 11, 12, 24]; however, in this case, no significant differences were detected in the distribution of these characteristics among the participants included in this study (severe obesity, obesity, and control groups). This eventuality allows the comparison of the results obtained, avoiding confounding factors. The age range selected in the different groups of participants was due to the fact that they usually have enough autonomy to carry out their extracurricular and/or leisure activities at these ages.
The higher prevalence of vitamin D deficiency in obesity has been sustained by several studies [9, 10, 11, 12], even though the potential mechanisms for this association still remain questionable. Nevertheless, at present, the most qualified hypotheses about the inverse relationship between vitamin D deficiency and obesity refer either to storage or sequestration of vitamin D in adipose tissue or volumetric dilution of vitamin D. Clinical studies have shown that obesity does not affect the cutaneous synthesis of vitamin D, but as it is a fat-soluble vitamin, it is accumulated and retained in the adipose tissue (storage site or sequestration hypothesis). Therefore, the greater the storage capacity of this vitamin in adipose tissue (severe obesity and obesity groups), the lower the serum levels of calcidiol [25, 26]. In fact, we found that calcidiol levels in the participants included in this study (severe obesity, obesity, and control groups) were inversely correlated with body mass index; this is an anthropometric measurement that has been frequently used in the diagnosis and follow-up of children and adolescents with obesity since it shows a good correlation with body fat content [27, 28]. A second probable mechanism of the inverse relationship between vitamin D deficiency and obesity could be a volumetric dilution; that is, vitamin D would be distributed in body compartments that increase with obesity (serum, fatty tissue, liver, etc.), thereby making serum levels lower [13, 15]. It has also been suggested that lower levels of calcidiol in obese patients could be due to impaired hepatic 25-hydroxylation related to nonalcoholic fatty liver disease, a condition that is common in obese adults but less frequent in childhood obesity [29]. However, none of the previously mentioned hypotheses would explain by itself, for example, the stronger trend to vitamin D deficiency in patients with obesity (severe obesity and obesity groups) living in urban areas than in those living in rural areas, as we identified in this study.
Vitamin D receptors are present in a large variety of tissues and cells in the body (muscle, heart, blood vessels, neurons, immune cells, breast, colon, prostate, etc.), and additionally, they have the capacity to produce calcitriol from circulating calcidiol. This fact supports the biological importance of sufficient calcidiol serum levels [1, 22]. Moreover, adipose tissue also expresses vitamin D receptors, and 1α-hydroxylase enzyme locally converts calcidiol to calcitriol (biological active form of vitamin D), and that process is not regulated by parathyroid hormone, in contrast with renal 1α-hydroxylase [30]. Additionally, some experimental data support that vitamin D could have an antiobesity effect by inhibiting adipogenesis during early adipocyte differentiation and independently of PTH. That is, vitamin D might be implicated in the pathogenesis of obesity, rather than being a consequence [3, 16]. These findings suggest, on one side, that adipose tissue could play a role in vitamin D metabolism rather than being a passive store of fat-soluble nutrients and, on the other side, that a bidirectional causal relationship between vitamin D deficiency and obesity cannot be excluded. However, several studies have shown no effect of vitamin D treatment on reducing body weight and/or body composition, suggesting that although vitamin D deficiency is associated with obesity, it is not bidirectional [31, 32].
In accordance with most authors [9, 10, 12, 24], we found a negative correlation between PTH and calcidiol levels, and this would be consistent with the physiological feedback mechanism of vitamin D on PTH secretion. But, interestingly, it is worth noting our finding that PTH levels were also significantly higher—independent of vitamin D status—in the patients with obesity (severe obesity and obesity groups) with respect to the control group. Many researchers have postulated that this elevation of PTH might increase calcium influx into adipocytes, which then leads to increased lipogenesis and potentially reduces catecholamine-induced lipolysis and, consequently, fosters fat storage [33, 34]. Additionally, several observational studies have shown that PTH levels in obesity are independent of vitamin D status, and it does not represent, as is commonly assumed, secondary hyperparathyroidism from hypovitaminosis D [35]. However, despite the above biological assumptions that obesity is related with vitamin D deficiency and elevated parathyroid hormone levels, the reason given for this association remains unexplained. In fact, some authors are currently questioning whether vitamin D deficiency is a consequence or cause of obesity [16], or whether the association between obesity and vitamin D deficiency is causality or casualty [3].
Obviously, unhealthy eating habits are related to childhood obesity, and this entails a lower intake of vitamin D. However, the main source of vitamin D is exposure to natural sunlight, while approximately 10% comes from natural dietary sources [1, 2]. Few foods naturally contain vitamin D (oily fish such as salmon, sardines, mackerel, and tuna, as well as shiitake mushrooms and eggs yolk) and, depending on the country, additional sources include fortified foods such as dairy products, orange juice, breakfast cereals, cookies, and butter or margarine [2, 36]. Therefore, even though diet seems to be probably an irrelevant factor in the acquisition of optimal levels of vitamin D, it could not be completely excluded.
Because geographical conditions affect body vitamin D levels, we cannot refer to a vitamin D status in a determined population without mentioning them. In our case, it should be noted that Navarre is a Spanish region located in the north of the Iberian peninsula with a population of 661,537 inhabitants (2021 census, National Institute of Statistics), 58.1% of whom live in urban areas and 41.9% in rural areas. Besides, it is characterized by a high frequency of precipitations and/or cloudiness and, especially, a high latitude (between 41°55″22 and 43°16″42 North). When the zenith angle of the sun is oblique, as occurs in the winter months in both hemispheres, type B ultraviolet radiation barely reaches the earth’s surface above and below 40°N and 40°S latitude, causing a very low or absence cutaneous synthesis of vitamin D, even with prolonged sun exposure [17, 22, 23]. In compliance with several studies [9, 24, 37, 38], this is a potential explanation for the seasonal variations in the prevalence of vitamin D deficiency (maximum prevalence in the winter months and minimum in the summer months) that we found in the control group.
Recent studies using personal electronic ultraviolet radiation dosimeters have displayed higher ultraviolet radiation exposure in children and adolescents living in rural areas compared with those living in urban areas due to differences in types of activity. Children and adolescents living in rural areas spend more time after school and during weekdays practicing outdoors chores during peak ultraviolet radiation hours (10 am–4 pm), compared with those living in urban areas who spend more time participating in indoor sports and/or leisure activities and, therefore, reducing exposure to sunlight [18, 19]. These data allowed us to hypothesize a much simpler explanation for the relationship between obesity and vitamin D deficiency: behavioral factors (outdoor activities and sun exposure) would be determined in reduced body content of vitamin D in patients with obesity.
Indeed, we also found seasonal variations in the prevalence of vitamin D deficiency (maximum prevalence in the winter months and minimum in the summer months) in patients with obesity (obesity and severe obesity groups), although showing significantly lower values with respect to control group. That is, on the one hand, this would confirm that sunlight exposure has a large impact on vitamin D status also in patients with obesity and, on the other hand, we found a stronger trend to vitamin D deficiency in patients with obesity (obesity and severe obesity groups) living in urban areas than in those living in rural areas. No significant differences were observed in the prevalence of vitamin D deficiency in the control group in relation to place of residence (urban or rural). Nevertheless, the most remarkable finding of this study was that patients with obesity (obesity and severe obesity groups) living in urban residence did not present significant seasonal variations in vitamin D deficiency throughout the year in contrast to those patients with obesity (obesity and severe obesity) living in rural residence, who presented a maximum prevalence of vitamin D deficiency in the winter months and a minimum in the summer months. Therefore, these findings would support the hypothesis that the greater tendency to present vitamin D deficiency in obese children and adolescents would be related to a sedentary lifestyle and, consequently, to the lack of adequate sun exposure. Otherwise, the participants of the control group, who presumably did not have a sedentary lifestyle, showed no differences in vitamin D status in relation to the place of residence (rural or urban).
At present, and despite the hypotheses recounted above, vitamin D photobiology suggests that the most probable mechanism for vitamin D deficiency in children and adolescents with obesity, rather than altered metabolic (sequestration in adipose tissue, volumetric dilution, impaired hepatic 25-hydroylation, etc.), is the behavioral factors (reduced sunlight exposure), such as our findings outline. However, other mechanisms cannot be completely excluded, as they may contribute concurrently.
The authors received no financial support for the research, authorship, and/or publication of this article (none declared).
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Written By
Teodoro Durá-Travé and Fidel Gallinas-Victoriano
Submitted: 26 April 2022Reviewed: 13 June 2022Published: 01 July 2022
Open access peer-reviewed chapter
